Classification Classification • Class 1• Class 2• Class 3• Class 4

Class 1Class 1• 1a• 1b• 1c

Class 1AClass 1A• Quinidine• Procainamide• Dysopyramide

Action of 1AAction of 1A• Open state Na channel blockers• Moderate delay on channel recovery-

1-10 sec• Suppress A-V conduction• Prolong refractoriness• Na channel blocking greater at high

frequency• Alpha blocker

Use of 1AUse of 1A• Ectopics• Re-entry-UDBBDB

EffectsEffects• Moderate phase o depression• Prolonged APD• Prolongs ERD

Suppress A-V conduction

Quinidine Quinidine • Na channel blockade• Antivagal action –inc atrial ERP---

reduce disparity among atrial ERP• Inc AV nodal ERP---but here this

effect is countered by anti vagal action

• Depress myocardial contractility---may cause CHF

Quinidine on ECGQuinidine on ECG• Inc PR• Inc QT• Changes in the shape of T wave

MOA of quinidineMOA of quinidine• Na channel block in open state---

reduce automaticity….• Reduce phase o depolerisation• Prolongs APD---K channel block• Inc ERP – due to moderate effect on

recovery on Na and K channels• High conc—inhibit Ca channel

Use of quinidineUse of quinidine• VT• SVT

ADRADR• TDP• Cardiac arrest• VF

interactionsinteractions• Inc digoxin toxicity• Hypotn• Risk of TDP is increasd by

hypokalemia by diuretics• Synergestic cardiac depression with

beta blockers, CCB,K salts

ProcainamideProcainamide• Orally active• Cardiac electro physiology is almost

identical to quinidine

Difference form quinidineDifference form quinidine1. Less effect in suppressing ectopic

automaticity2. Less marked depression of

contractility and AV conduction3. Anti vagal action is minimal4. Not an alpha blocker

PKPK• Oral BA- 75%• Met by liver ---N acetyl

Procainamide---NAPA--- no Na blocker• NAPA---K blocker• Dose 0.5-1 g• ADR-cardiotoxic,TDP

Major side effect of Major side effect of ProcainamideProcainamide

• SLE in 1/5th of pateints• Presence of Anti Nuclear Antibodies

• Use –Monomorphic VT,WPW---i.v.

DysopyramideDysopyramide• Quinidine like• Prominent cardiac depressent• Anticholinergic• No alpha block• C/I- sick sinus,CHF,Prostatic

hypertrophy

Class 1BClass 1B• Drugs block Na channel• More in inactivated stage• Do not delay recovery• No AV conduction depression• Shortens APD,ERP,QT

• Eg.---Lidocaine

Lignocaine-LidocaineLignocaine-Lidocaine• Supress automaticity in ectopic foci• Antogonize----phase 4 depolerisation

and after depolerization---in PF• SA node automaticity is not

depressed• Phase 0 dep and cond vel of AV

bundl and ventricles---not decreased

• Red—APD---PF,Ventricles• No effect on APD and ERP of atrial

fibres• Atrial re-entry is not affected

• Suppress ventricular re-entry

MOA of lignocaineMOA of lignocaine• Block inactivated Na channels• Relatively selective for partially

depolarised cells and with longer APD• Nl ventricular conducting fibres- not

affected• Not effective in atrial arrythmias• Minimal effect on ECG• No depression of contractility/BP

Pk Pk • Orally inactive ---high first pas met• i.v. bolus• 50-100 mg bolus followed by 20-40

mg every 20 min

ADR—of lignocaineADR—of lignocaine• Neurological effects—

drowsines,nausea,blurre vision• No pro arrythmic effect• Least cardio toxic

Use of lignocaineUse of lignocaine• Only in VA1. A following acute MI2. Cardiac surgery3. Used in digitalis toxicity as does not

worsen A-V block

1c1c• Most potent Na channel blockers• More action on open• Longest recovery time• Markedly delay conduction• Prolong P-R• Broaden QRS complex• APD not affected

Class 2Class 2• Beta blockers